June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
The Effect of Interleukin 38 on Angiogenesis in a Model of Oxygen-induced Retinopathy
Author Affiliations & Notes
  • Jing Zhang
    Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China
  • Shaobo Su
    Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China
  • Footnotes
    Commercial Relationships   Jing Zhang, None; Shaobo Su, None
  • Footnotes
    Support  31471122 from the National Natural Science Foundation of China
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 208. doi:
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      Jing Zhang, Shaobo Su; The Effect of Interleukin 38 on Angiogenesis in a Model of Oxygen-induced Retinopathy. Invest. Ophthalmol. Vis. Sci. 2017;58(8):208.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose : Interleukin 38 (IL-38) is a novel identified cytokine of IL-1 family in which some members are important in inflammation and angiogenesis. However, the role of IL-38 in angiogenesis is unknown. The aim of the present study is to explore the effect of IL-38 on angiogenesis.

Methods : Mouse oxygen-induced retinopathy (OIR) model was induced of by exposure of hyperoxia (75% oxygen) to C57BL/6J mice from postnatal day 7 (P7) to P12 and then returned to room air. The mice were intravitreal injection with 1μl of IL-38 dissolved at different concentrations (0, 5, or 25 ng/μl) at P12. At P17, neovascular region (tufts) and avascular area were analyzed. In addition, the effect of IL-38 on the migration, proliferation and tube formation were examined by human umbilical vein endothelial cells (HUVECs) in vitro.

Results : In vitro, IL-38 was expressed in endothelial cells and was down-regulated under hypoxic condition. IL-38 reduced the proliferation, migration and tube formation of endothelial cells in a dose-dependent manner. In vivo, IL-38 was expressed in mouse retina. Neonatal mice administrated with IL-38 in a mouse model of oxygen-induced retinopathy (OIR) showed that retina neovascularization was reduced.

Conclusions : Our findings suggest that IL-38 is an antiangiogenic cytokine in pathophysiological settings.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.


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